Relationship between IMoninvasive Cardiopulmonary Exercise Testing and Central Hemodynamics in Patients with Severe Chronic Heart Failure

Abstract

In view of the frequent follow-up evaluations of patients with severe chronic heart failure, the purpose of this study was to assess whether noninvasive gas exchange parameters from cardiopulmonary exercise testing (CPX), measured at ventilatory threshold (VT), are related to invasively measured peak diastolic pulmonary artery pressure (dPAP) and peak cardiac output (CO). 23 males with severe chronic heart failure underwent CPX on a bicycle ergometer (supine; steps of 25 W/5 min) during right heart catheterization. dPAP and/or CO increased significantly from rest to VT (18 ±10-9 30 ±10 mm Hg, p < 0.01; 4.8 ± 1.4 -9 6.4 ± 2.3 liters/min, p< 0.05), but did not from VT to peak exercise (33 ± 10 mm Hg; 7.3 ± 2.5 liters/min). Data indicated severely deteriorated hemodynamics at rest and during exercise. Oxygen uptake (VO2) increased from rest (270 ± 45 ml/min) to VT (650 ± 135 ml/min at 27 ± 7 W) to peak exercise (829 ± 183 ml/min at 39 ± 23 W). VO2 data were normal for a given workload. From all CPX data at VT, only 02 pulse correlated with peak dPAP (r = -0.58; p < 0.05). Peak CO correlated with O2 pulse (r = -0.49), VO2 (r = 0.46), ventilatory equivalent for O2 (r = -0.43) and tidal volume (r = 0.43), measured at VT (p < 0.05 for all parameters). Variance of peak dPAP and peak CO could only be explained by O2 pulse at VT (58 and 49%, respectively). Noninvasive cardiopulmonary data at VT did not give sufficient information about peak dPAP and peak CO in patients with severe chronic heart failure using a steady-state protocol. This indicates that early ventilatory threshold should not be considered indicative of reduced CO due to skeletal muscle underperfusion in heart failure patients.